Hoshang J. Khambatta

Myocardial ischemia in untreated hypertensive patients: effect of a single small oral dose of a beta-adrenergic blocking agent

In a non-double-blind, prospective, randomized study, the intraoperative electrocardiograms of 128 mildly hypertensive surgical patients were examined in order to determine the incidence of myocardial ischemia during anesthesia. No patient had been receiving chronic antihypertensive therapy prior to the study, but a single small oral dose of a beat-adrenergic blocking agent (labetalol, atenolol, or oxprenolol) was given to 89 of them along with premedication-Forty-four per cent of the untreated control patients and 61% of the patients pretreated with a beat-adrenergic blocking agent had normal preoperative electroca rdiograms and no risk factors for coronary artery disease other than hypertension (this difference between groups was not statistically significant). During tracheal intubation and/or emergence from anesthesia, a brief, self-limited episode of myocardial ischemia was detected in 11 of 39 untreated control patients, and in two of 89 patients pretreated with a betaadrenergic blocking agent (P < 0.001). Tachycardia always accompanied the ischemic events, but a conspicuous increase in blood pressure did not. The authors conclude that mild hypertension, when untereated prior to the induction of anesthesia, is associated with a high incidence of myocardial ischemia; and that a single small oral dose of a beat-adrenergic blocking agent, given with premedication, can significantly reduce that risk.

Hypertension during anesthesia on discontinuation of sodium nitroprusside-induced hypotension.

The authors had observed that on intraoperative discontinuation of sodium nitroprusside being administered to induce hypotension, mean arterial pressure increased to above the pre-hypotension level. Twelve patients who received hypotensive anesthesia for surgical correction of cerebral aneurysms were studied to evaluate the role of the renin–angiotensin system in this phenomenon. In the awake state, mean arterial pressure was 100 ± 2 torr and plasma renin activity 3.0 ± 0.1 ng/ml/hr. Thirty minutes after the establishment of stable halothane–nitrous oxide anesthesia, mean arterial pressure decreased to 85 ± 1 torr and plasma renin activity increased to 4.4 ± 0.1 ng/ml/hr. No appreciable change in either occurred over the next two hours of operation. During sodium nitroprusside-induced hypotension, mean arterial pressure decreased to 49 ± 2 torr and plasma renin activity increased to 15.2 ± 0.2 ng/ml/hr. Thirty minutes after discontinuation of sodium nitroprusside administration, mean arterial pressure increased to 112 ± 2 torr, which was not only higher than the prehypotension level, but also significantly higher than that recorded in the awake state. Plasma renin activity at that time was 10.9 ± 0.1 ng/ml/hr. As the half-life of plasma renin is 15 min, the data suggest that the persistently increased plasma renin activity is probably responsible for the increase of arterial pressure following sodium nitroprusside-induced hypotension.

Pulmonary Shunting during Anesthesia with Deliberate Hypotension

Pulmonary shunling (&OV0422;t,/&OV0422;t, with FIO2 = 1) was measured in 18 anesthetized patients during deliberate hypotension. Hypotension was induced in 12 patients with sodium nitroprusside and light halothane anesthesia and in six others with deep halothane anesthesia and mechanical hyperventilation. Similar results were observed in the two groups. During the hypotensive period mean arterial pressure (MAP) was reduced to 49 ± 2 torr, a 37 per cent decrease from the control level after the onset of operation and a 40 per cent decrease compared with the recovery level during closure of the wound. &OV0422;t/&OV0422;t, however, remained unchanged throughout the study; 52 ± 0.9 per cent initially, 5.4 ± 0.8 per cent during hypotension, and 4.7 ± 0.5 per cent during recovery. It is concluded that pulmonary shunting need not develop during dliberate hypotension induced with either technique.

Global and regional myocardial blood flow and metabolism during equipotent halothane and isoflurane anesthesia in patients with coronary artery disease.

Global and regional myocardial blood flow and metabolism were examined in 20 patients with coronary artery disease before surgical stimulation. Half were anesthetized with halothane (0.8%) and half with isoflurane (1.2%). Coronary perfusion pressure decreased similarly in both groups. During halothane anesthesia coronary sinus blood flow, an index of global perfusion, decreased from an awake value of 129 ± 7 to 97 ± 7 ml/win (P < 0.05), and great cardiac rein blood flow, an index of regional perfusion, decreased from 60 ± 8 to 44 ± 5 ml/mm (P < 0.05). In contrast, during isoflurane anesthesia global coronary blood fine increased from 131 ± 13 to 153 ± 16 ml/min (P < 0.05), while regional blood flow decreased from 68 ± 7 to 56 ± 6 mVmin (P < 0.05). Thus, the ratio of great cardiac vein blood flow to coronary sinus blood flow was unchanged during halothane anesthesia but decreased significantly during isoflurane. Neither global nor regional coronary vascular resistance was altered by halothane, whereas isoflurane decreased global coronary vascular resistance without affecting regional coronary vascular resistance. All patients receiving halothane had net myocardial lactate extraction. In the isoflurane group, four patients showed global lactate production and three regional lactate production. All patients demonstrating lactate production also developed electrocardiographic evidence of myocardial ischemia, which was not present before induction. The authors conclude that halothane is a preferable anesthetic to isoflurane in patients with coronary artery disease because the latter has the propensity to induce maldistribution of the coronary circulation and myocardial ischemia.

Cerebrospinal Fluid Levels of d-Tubocurarine in Man

Using radioimmunoassay, d-tubocurarine (dTc) was found in the cerebrospinal fluid (CSF) of man after intravenous injection. When dTc was administered in a single dose (0.3 mg/kg) to nine patients, small quantities, 3.5 ±.26 ng/ml (mean ± SE), appeared in the lumbar CSF within 5 minutes. The concentration of dTc in the CSF remained constant for the next 25 minutes, but then began to increase with time to 9.3 ± 4.4 ng/ml 30 minutes after injection, 14.5 ± 4.4 ng/ml at one hour, and 24.9 ± 6.5 ng/ml at six hours. In another group of six patients, three doses of dTc (0.3 mg/kg) were given at 90-minute intervals. Concentration of dTc in the CSF increased after each injection. The quantities of dTc found in the CSF are unlikely to produce any pharmacologic or adverse effect (e.g., convulsion) in man.

Effects of respiratory alkalosis on oxygen consumption and oxygenation.

The effect of respiratory alkalosis on oxygen consumption after passive hyperventilation was studied in eight dogs. PaCo2 decreased from 32.1 to 13.6 torr, pH increased from 7.43 to 7.72, and oxygen consumption increased from 116.5 to 147.5 ml/m2/min. Venous admixture decreased from 17.1 to 8.8 per cent during passive hyperventilation, while cardiac index, PaO2, SaO2, and CaO2 did not change significantly. Using a model, it can be shown that if oxygen consumption did not increase, PaO2, SaO2, and CaO2 during hyperventilation would be higher than the values observed experimentally. The observed increase in VO2 during respiratory alkalosis prevents a maximal increase in arterial oxygenation in the normal animal.

Propranolol Alters Renin Release during Nitroprusside-induced Hypotension and Prevents Hypertension on Discontinuation of Nitroprusside

Ten patients who received hypotensive anesthesia for surgical correction of a cerebral aneurysm were pretreated for 1 day with propranolol. In the awake state, before start of anesthesia, mean arterial pressure was 91 +/- 3 torr and plasma renin activity 3.0 +/- 0.1 ng/ml/hr. Thirty minutes after the induction of anesthesia mean arterial pressure decreased to 79 +/- 2 torr and plasma renin activity increased to 3.5 +/- 0.1 ng/ml/hr. There was no further significant change in either measurement with surgical stimulation. During sodium nitroprusside-induced hypotension (the dose used was 0.35 +/- 0.02 mg/kg) mean arterial pressure was reduced to 53 +/- 2 torr, and plasma renin activity increased to 8.8 +/- 0.9 ng/ml/hr. Heart rate did not change. Discontinuation of sodium nitroprusside resulted in a gradual reduction of plasma renin activity to the awake level and concurrent gradual increase in mean arterial pressure to its basal anesthetic value. When compared with previous work, these results indicate that propranolol attenuates nitroprusside-induced renin release, reduces the dosage of nitroprusside required to induce hypotension, suppresses reflex tachycardia, and prevents overshoot hypertension on discontinuation of nitroprusside.

Propranolol premedication blunts stress response to nitroprusside hypotension.

Hypotension was induced in sixteen patients with nitroprusside during anesthesia for surgical correction of cerebral aneurysms. Eight patients were premedicated with propranolol (180 mg orally) for one day and the other eight were not. Before the start of anesthesia, the untreated patients had a mean arterial pressure of 102 ± 3 mm Hg, a heart rate of 76 ± 2 beats/min, and plasma epinephrine and norepinephrine concentrations of 114 ± 21 and 258 ± 34 pg/ml, respectively. The propranolol-premedicated patients came to the operating room in a significantly different clinical state with a mean arterial pressure of 92 ± 3 mm Hg, a heart rate of 71 ± 2 beats/min, and plasma epinephrine and norepinephrine concentrations of 76 ± 28 and 144 ± 28 pg/ml. During induced hypotension, plasma epinephrine and norepinephrine concentrations increased significiantly in both groups (454 ± 42 and 730 ± 58 pg/ml in the untreated patients, 160 ± 48 and 419 ± 67 pg/ml in the propranolol premeditated patients), but the increase in catecholamines was significantly greater in the untreated patients. Thirty minutes after nitroprusside was discontinued, epinephrine and norepinephrine concentrations were higher than in the awake state in untreated patients and were associated with rebound hypertension and tachycardia. In contrast, in propranolol-premedicated patients, plasma epinephrine and norepinephrine concentrations decreased towards the preanesthesia values, mean arterial pressure gradually returned to the prehypotension level, and heart rate remained unchanged. This study thus demonstrates that propranolol premedication attenuates the release of catecholamines in response to nitroprusside-induced hypotension.

Electrocardiographic Artifacts During Cardiopulmonary Bypass

An electrocardiogram (ECG) free from interference is today a necessity for safe anesthetic management. Electrocardiogram artifacts caused by surgical cautery units, power lines, and muscle twitching and fasciculation have been recognized (14). More recently, ECG interference has been observed during extracorporeal shock wave lithotripsy (5) and during crystalloid administration through a fluid warming apparatus (6). During cardiopulmonary bypass (CPB) we have been experiencing another type of ECG artifact, which has not yet been reported. The purpose of this paper is to describe the characteristics and incidence of this interference, and to suggest an etiology and possibly a solution to the problem.

Cardiac performance preserved despite thiopental loading.

BackgroundSome cerebral artery aneurysms require cardiopulmonary bypass and deep hypothermic circulatory arrest to be clipped safely. During bypass these neurosurgical patients often are given large doses of thiopental in the hope that additional cerebral protection will be provided. However, thiopental loading during bypass has been associated with subsequent cardiac dysfunction in patients with heart disease. This study was undertaken to determine how patients without concomitant heart disease would respond to thiopental loading. MethodsTwenty-four neurosurgical patients with giant cerebral aneurysms and little or no cardiac disease were anesthetized with fentanyl, nitrous oxide, and isoflurane. Thiopental was titrated to achieve electroencephalographic burst-suppression before bypass, and the infusion was continued until after separation. Prebypass hemodynamic and echocardiographic measurements were obtained during a stable baseline and 15 min after thiopental loading began. They were repeated after bypass. ResultsPrebypass thiopental loading increased heart rate from 61 ± 11 to 72 ± 13 beats/min and decreased stroke volume from 43 ± 10 to 38 ± 8 ml. beat−1. m-2, but arterial and filling pressures, vascular resistance, cardiac index, and ejection fraction remained the same. Before bypass, thiopental plasma concentration measured 28 ± 8